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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
1985-10-7
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pubmed:abstractText |
Insulin resistance and insulin deficiency are both present in many patients with diabetes mellitus. We tested the hypothesis that insulin resistance can evolve from a primary lesion of the beta-cell secretory function. Insulin-mediated glucose uptake (insulin clamp), endogenous glucose production, and glucose-stimulated insulin secretion (hyperglycemic clamp) were measured in awake dogs before and four to six weeks after streptozotocin-induced diabetes mellitus. Streptozotocin (30 mg/kg) resulted in a significant rise in the mean fasting plasma glucose concentration from 104 +/- 2 mg/100 mL to 200 +/- 34 mg/100 mL, (P less than 0.05), and a slight decrease in the mean fasting plasma insulin concentration (from 21 +/- 2 microU/mL to 15 +/- 2 microU/mL). Under conditions of steady-state hyperglycemia (+75 mg/100 mL hyperglycemic clamp, insulin secretion was reduced by 75% in the streptozotocin-treated dogs (P less than 0.025), and the total amount of glucose metabolized decreased from 13.56 +/- 1.04 to 4.74 +/- 0.70 mg/min X kg (P less than 0.001). In the postabsorptive state, endogenous glucose production was slightly, although not significantly, higher in the diabetic dogs (3.05 +/- 0.46 v 2.51 +/- 0.22 mg/min . kg), while the glucose clearance rate was 35% lower (P less than 0.001). When the plasma insulin concentration was increased to approximately 45 microU/mL (insulin clamp) while holding plasma glucose constant at the respective fasting levels (99 +/- 1 and 186 +/- 30 mg/100 mL), endogenous glucose production was completely suppressed in control dogs but suppressed by only 51% (1.46 +/- 0.37 mg/min . kg, P less than 0.025) in diabetic animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0026-0495
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
34
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
817-25
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:3897768-Animals,
pubmed-meshheading:3897768-Blood Glucose,
pubmed-meshheading:3897768-Diabetes Mellitus, Experimental,
pubmed-meshheading:3897768-Dogs,
pubmed-meshheading:3897768-Fasting,
pubmed-meshheading:3897768-Glucose,
pubmed-meshheading:3897768-Hyperglycemia,
pubmed-meshheading:3897768-Insulin,
pubmed-meshheading:3897768-Insulin Resistance,
pubmed-meshheading:3897768-Islets of Langerhans,
pubmed-meshheading:3897768-Liver,
pubmed-meshheading:3897768-Monocytes,
pubmed-meshheading:3897768-Perfusion,
pubmed-meshheading:3897768-Receptor, Insulin
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pubmed:year |
1985
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pubmed:articleTitle |
Hepatic and peripheral insulin resistance following streptozotocin-induced insulin deficiency in the dog.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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